Licata S P, Werber A H, Hough L B
Department of Pharmacology and Toxicology, Albany Medical College, NY 12208.
Physiol Behav. 1988;42(6):563-8. doi: 10.1016/0031-9384(88)90158-8.
Because previous studies have suggested that activation of baroreceptors could mediate stress-induced analgesia, the effect of acute exposure to footshock on mean arterial pressure (MAP) and pain sensitivity was simultaneously determined in conscious rats receiving the histamine H2 receptor antagonist cimetidine or vehicle. Continuous exposure to 3 min of inescapable footshock (3.5 mA) dramatically decreased pain sensitivity, with no increase in post-stress MAP, when compared to no shock controls. The histamine H2-antagonist cimetidine (100 mg/kg, IP) had no significant effect on MAP in resting or stressed animals, but inhibited the stress-induced analgesia, showing that the antagonism of the analgesia is not mediated by modulation of post-stress MAP. Although footshock failed to elicit a significant increase in MAP, a highly significant correlation was found between individual analgesic scores and shock-induced pressure changes in animals treated with cimetidine; in animals receiving vehicle, no such correlation was observed, although the use of a cutoff in analgesic testing may explain this. These results suggest the existence of a stress-induced analgesic mechanism resistant to cimetidine, but associated with elevated MAP.
因为先前的研究表明压力感受器的激活可介导应激诱导的镇痛作用，所以我们在接受组胺H2受体拮抗剂西咪替丁或赋形剂的清醒大鼠中，同时测定了急性足部电击对平均动脉压（MAP）和疼痛敏感性的影响。与无电击对照组相比，持续暴露于3分钟无法逃避的足部电击（3.5 mA）可显著降低疼痛敏感性，应激后MAP无升高。组胺H2拮抗剂西咪替丁（100 mg/kg，腹腔注射）对静息或应激动物的MAP无显著影响，但可抑制应激诱导的镇痛作用，表明镇痛作用的拮抗不是通过调节应激后MAP介导的。尽管足部电击未能引起MAP显著升高，但在用西咪替丁治疗的动物中，个体镇痛评分与电击诱导的压力变化之间存在高度显著的相关性；在接受赋形剂的动物中，未观察到这种相关性，尽管在镇痛测试中使用临界值可能解释了这一点。这些结果表明存在一种对西咪替丁有抗性但与MAP升高相关的应激诱导镇痛机制。
